Kraj: Kanada
Język: angielski
Źródło: Health Canada
ACYCLOVIR (ACYCLOVIR SODIUM)
AURO PHARMA INC
J05AB01
ACYCLOVIR
50MG
SOLUTION
ACYCLOVIR (ACYCLOVIR SODIUM) 50MG
INTRAVENOUS
15G/50G
Prescription
NUCLEOSIDES AND NUCLEOTIDES
Active ingredient group (AIG) number: 0115506007; AHFS:
APPROVED
2019-12-03
PRODUCT MONOGRAPH PR ACYCLOVIR SODIUM INJECTION (50 mg Acyclovir/mL) House Standard Antiviral Agent AURO PHARMA INC. Date of Preparation: 3700 Steeles Avenue West, Suite # 402 November 29, 2019 Woodbridge, Ontario, L4L 8K8 CANADA Submission Control No.: 215417 PR ACYCLOVIR SODIUM INJECTION 50 mg Acyclovir/mL House Standard THERAPEUTIC CLASSIFICATION Antiviral ACTION AND CLINICAL PHARMACOLOGY Acyclovir, a synthetic acyclic purine nucleoside analog, is a substrate with a high degree of specificity for herpes simplex and varicella-zoster-specified thymidine kinase. Acyclovir is a poor substrate for host cell-specified thymidine kinase. Herpes simplex and varicella-zoster-specified thymidine kinase transform acyclovir to its monophosphate which is then transformed by a number of cellular enzymes to acyclovir diphosphate and acyclovir triphosphate. Acyclovir triphosphate is both an inhibitor of, and a substrate for, herpes virus-specified DNA polymerase. Although the cellular α-DNA polymerase in infected cells may also be inhibited by acyclovir triphosphate, this occurs only at concentrations of acyclovir triphosphate which are higher than those which inhibit the herpes virus-specified DNA polymerase. Acyclovir is selectively converted to its active form in herpes virus infected cells and is thus preferentially taken up by these cells. Acyclovir has demonstrated a very much lower toxic potential _in vitro _for normal uninfected cells because: 1) less is taken up; 2) less is converted to the active form; 3) cellular α-DNA polymerase has a lower sensitivity to the action of the active form of the drug. A combination of the thymidine kinase specificity, inhibition of DNA polymerase and premature termination of DNA synthesis results in inhibition of herpes virus replication. No effect on latent nonreplicating virus has been demonstrated. Inhibition of the virus reduces the period of viral shedding, limits the degree of spread and level of pathology, and thereby facilitates healing. During suppression, there is no eviden Przeczytaj cały dokument